Area of research
Cardiology and Cardiovascular Medicine · Molecular Biology
Research interest
Research interests include Cardiomyopathy and Myosin Studies, Cardiovascular Effects of Exercise, Muscle Physiology and Disorders, and Cardiovascular Function and Risk Factors.
Heterogeneous Dysregulation of Myosin Super-Relaxation and Energetics in Hypertrophic Cardiomyopathy
The role of the troponin T interactions with actin in regulation of cardiac thin filament revealed by the troponin T pathogenic variant Ile79Asn
Phenotype specific nuclear lamina remodeling in hiPSC derived cardiomyocytes bearing TNNT2 sarcomeric variants
A Central Role for Troponin C Amino-Terminal α-Helix in Vertebrate Thin Filament Ca2+-Activation
Troponin Structural Dynamics in the Native Cardiac Thin Filament Revealed by Cryo Electron Microscopy
Structure of mavacamten-free human cardiac thick filaments within the sarcomere by cryoelectron tomography
Post‐translational modifications of vertebrate striated muscle myosin heavy chains
Can evolution-based studies inform modern medicine?
ATP-induced reconfiguration of the micro-viscoelasticity of cardiac and skeletal myosin solutions
Cardiac troponin T N-domain variant destabilizes the actin interface resulting in disturbed myofilament function
Suppression of lusitropy as a disease mechanism in cardiomyopathies
Etiology of genetic muscle disorders induced by mutations in fast and slow skeletal MyBP-C paralogs
Nucleus Mechanosensing in Cardiomyocytes
Disruption of Z-Disc Function Promotes Mechanical Dysfunction in Human Myocardium: Evidence for a Dual Myofilament Modulatory Role by Alpha-Actinin 2
Unlocking the Role of sMyBP-C: A Key Player in Skeletal Muscle Development and Growth
Micro-mechanical response and power-law exponents from the longitudinal fluctuations of F-actin solutions
High-resolution cryo-EM structure of the junction region of the native cardiac thin filament in relaxed state
Myofibril orientation as a metric for characterizing heart disease
Arrhythmogenic Cardiomyopathy: Exercise Pitfalls, Role of Connexin-43, and Moving beyond Antiarrhythmics
Efficacy and Safety of Angiotensin Receptor Blockers in a Pre-Clinical Model of Arrhythmogenic Cardiomyopathy
Low expression of the K280N TNNT2 mutation is sufficient to increase basal myofilament activation in human hypertrophy cardiomyopathy
Hypertrophic and dilated cardiomyopathy-associatedTNNT2 pathogenic variants induce nucleus remodeling in hiPSC-CM models
Phosphomimetic mutations in the C-terminal basic region of troponin T increases actin filament activity
Modeling force redevelopment as a response to thin filament activation time
Role of cardiac alpha-actinin 2 pathogenic variant in human myocardium mechanics
The HCM I79N pathogenic variant in cardiac TNT induces thick filament malfunction and myofilament lattice rearrangement
Mechanism(s) of regulation of the cardiac thin filament: new perspectives for a longstanding enigma
The structure of the native cardiac thin filament at systolic Ca <sup>2+</sup> levels
Fast skeletal myosin-binding protein-C regulates fast skeletal muscle contraction
Pathogenic variants in TNNC2 cause congenital myopathy due to an impaired force response to calcium